CLRs can directly recognize and tether pathogens (viruses, fungi, and bacteria) to the cell surface, inducing intracellular signaling cascades that mediate pathogen uptake and killing, production of inflammatory mediators, and the induction of several other protective cellular responses, including the respiratory burst (ROS) and NET formation. CLRs can promote antigen (cross-) presentation and shape the development of adaptive immunity (including Th1, Th17, and CTL responses). The functions of CLRs can also be detrimental, for example, by altering the expression of other key PRRs, inhibiting antigen presentation, directly facilitating viral infection of myeloid cells, and promoting pathological inflammation, including Th2 responses in the context of allergy. The impact of pathogen recognition by CLRs can also be indirect, for example, by induction of immunomodulatory cytokines and other mediators. It is important to note that the outcome of infection involves recognition of pathogens through multiple PRRs whose intracellular signaling pathways integrate in ways that are incompletely understood. The role of CLRs in anti-parasite immunity is less clear.
